The most commonly ordered (chemistry) laboratory investigation s Deborah Hillman White, 4 th year student, PMS Doctors as Teachers SSU 2007
The most commonly
ordered (chemistry) laboratory
investigations
Deborah Hillman White, 4th year student, PMS
Doctors as Teachers SSU 2007
Day 1
Course objectives
• To provide participants with the knowledge required to:– Run the appropriate tests– Select the correct boxes and blood bottles– Facilitate diagnosis– Understand why electrolyte imbalances lead to
body s/s– Know the key s/s associated with derangements– Understand treatment principles – Comprehend test limitations
Investigations covered in this course
1. Sodium2. Potassium3. Calcium4. Magnesiu
m5. Phosphate6. Chloride7. Creatinine8. Urea
9. Amylase10.T. Proteins (= albumin +
globulin)
11. ALT12. AST13. ALP14. T.
Bilirubin15. gGT
Fun, fun, fun exercise no. 1
It’s your first day of F1 on EMU…and you’ve got the job assisting the ward monkey. During the morning round, they request that you “take bloods from bed 3, fill-out ‘the form’ and send it to the lab in the pod – do FBC, U&Es and a bone study”.
1. What boxes are you going to tick?2. Exactly what electrolytes are you testing when you
test for U&Es?3. What tests are conducted as part of a ‘bone study’?4. (Additionally) What is tested when you mark the box
entitled, ‘renal’? 5. What is tested when you mark the box entitled, ‘Liver’
Punxsutawney Phil says
• Order only when necessary• Interpret results within
context• Repeat deranged tests if
possible• COMPLETELY fill it in• Confine the alphabet to the
boxes• Use a new form if you
make a mistake
Sodium (Na)
Na – source, storage, functions
• Source: diet• Storage: most abundant EC cation• Functions:
1.Primary determinant of extracellular volume
2.Key solute influencing the osmotic pressure of the interstitial fluid
3. Nerve and muscle function
Na - regulation
• Two mechanisms involved– ECF volume (& BP) – kidneys (RAA) / ANP– Plasma osmolality – vasopressin
• Plasma Na not closely correlated to Na excretion
– Think of two separate systems1. volume control2. osmoregulation
– Sometimes, both systems activated (SIADH)
High LowVolume / pressure (factors:
circ. vol. & resistance)
ANP released–increases GFR and Na filtration–deactivates RAA system
1. Baroreceptors activate
catecholamines.
2. JGA activates RAA cascade
Osmoregulation
Osmolality sensed by
osmoreceptors– thirst–vasopressin
Dec. vasopressin =
dec. water reabsorption =
dilute urine
Na – clinical scenario examples
Volume/pressure regulators
Water / osmoregulation
Scenario RAA ANP V.pressin
Thirst Result
Admin. isotonic saline
-
↑- - Excretion of Na
load in appropriate amount of iso-osmotic urine
Ingestion of salty nuts (!)
↓ ↑ ↑ ↑ Excretion of
concentrated urine (both systems activated)
SIADH
↓ ↑ ↑ ↓ Excretion of
concentrated urine in presence of relative hyponatraemia
Na – signs and symptoms
Fatigue, weakness, headache, nausea
When it’s serious: confusion, coma, convulsions, death
Fatigue, weakness, headache, nausea
When it’s serious: confusion, coma, convulsions, death+ muscle twitching
High Low
Causes of hypernatraemia
High intake / producti
on
Administration of hypertonic solutions or drugs (e.g. saline)
Reduced excretio
n
Primary aldosteronism Renal failure Drugs – NSAIDs,
mineralcorticoids
Other Impaired thirst / conscious state Diabetes insipid us Water loss: burns, vomit,
diarrhoea etc. Osmotic diuresis – e.g. DKA
Causes of hyponatraemiaIs the patient dehydrated?
Is the urinary Na >20mmol/L?
NoYes
Is the patient oedematous
Yes (i.e. kidney
loss)
•Addisons
•Diuretics
•Osmotic diuresis
No (i.e. extrarenal
loss)
•D&V
•Burns
•Obstruction
•Trauma – post -op
•Heat
•CF
No
•Water overload
•Glucocorticoid insufficiency
•Severe hypothyroidism
No
Is urine osmolality >500 mmol/kg?
Yes
•SIADH
Yes
•Nephrotic syndrome
•Cardiac failure
•Cirrhosis
•Renal failure
TreatmentHypernatraemia – • Tx underlying disease • H2O, dextrose 5% IVI• Sometimes 0.9% recommended, as hypotonic in a
hypernatraemic patient (less marked fluid shifts)• Also vasopressin analogues sometime given.
Hyponatraemia – • Tx underlying disease (Don’t use plasma Na as guide)• In hypervolaemic hyponatraemia emergencies - saline +/- a
diuretic (e.g. furosemide). Treat SLOWLY (1-2 mmol/L/hour). Caution: central pontine myelinolysis.
• Patients with vomiting / severe volume depletion - intravenous normal saline with K supplements
• SIADH - fluid restrict
Na – summary points
Potassium (K)
K – source, storage, functions
• Source: diet• Storage: most intracellular cation• Functions:
– Key determinant of cell membrane potential • Fundamental for normal nerve and muscle
function• Important role in kidney function • Essential for protein and nucleic acid synthesis • Converts glucose into glycogen (muscle fuel) • Needed to maintain acid/alkali balance
K - regulation
• Aldosterone – affects two sites involved in K homeostasis:– Kidney– GI tract
• Affected by acid base balance, catecholamines and insulin
K – signs and symptoms
Cardiac excitability arrhythmias, decreased cardiac contractility
Muscle function hypotonia, lethargy, muscle weakness, cramps
Cardiac excitability rapid HR, VF, arrhythmias, ECG changes
High Low
Causes of hyperkalaemia
High intake / producti
on
Blood transfusions LoSalt
Reduced excretio
n
Renal failure Drugs – diuretics, ACEi Aldosterone deficiency / Addisons
Redistribution
Hormones Acidosis Cell death – burns, chemotherapy
Other Artefact - venepuncture technique Physiological – pregnancy,
standing, AM
Causes of hypokalaemia
Low intake / producti
on
Hypokalaemic IV therapy Ileus Intestinal obstruction Anorexia
Increased excretio
n
Drugs – diuretics, purgatives Aldosterone 2o to CCF, liver
failure Endocrine problems: Cushings,
Conns D&V
Redistribution
Hormones – insulin, cortisol B adrenergic stimulation – B2
agonist nebs Metabolic alkalosis
TreatmentHyperkalaemia – • Emergency treatment (ECG changes present)
1. Protect myocardium– 10ml calcium gluconate 10%
2. Drive K into cells – 10 –20 units insulin + 50mls 50% dextrose IV (repeat as
necessary)– Nebulised salbutamol 2.5mg
3. (If appropriate) correct acidosis (ph <6.9) – Sodium bicarbonate
4. Deplete body K (After emergency treatment) – Polystyrene sulphonate resin 15g orally 3/day with laxatives or
30g rectally followed after 3-6 hours with an enema5.5. Renal replacement therapy if required
Hypokalaemia – • Treat underlying disease• If mild, increase dietary intake (fruit, vegetables) or oral K
supplements • If severe, give IV K cautiously
K – summary points
Fun, fun, fun exercise no. 2
It’s now 10 minutes into the first day of F1 on EMU…and the SHO has been bleeped just as they were finishing-off writing out a pathology request form. They ask you to take “take bloods from side room 5 for the requests that are on the form”. You see the following boxes have been marked: renal, liver, coag screen, glucose.
1. How many blood bottles do you need?2. What colour are they?
Calcium (Ca)
Ca – source, storage, functions
• Source: diet• Storage: Skeleton, teeth (99%), intracellular, ECF
• Transport: Bound to plasma proteins and PO. Free portion regulated.
• Functions: – Neuromuscular excitability – Excitation-contraction coupling- cardiac / smooth
muscle – Stimulus-secretion coupling– Maintenance of tight cell junctions– Blood clotting– Structural / functional integrity of bones, teeth etc.
Ca – signs and symptoms
Neuromuscular excitability – Tetany (Chvosek’s)– Muscle
cramps/spasms (Trousseau’s)
– AsphyxiationExcitation-
contraction – ECG changes
Bone/teeth integrity– Short stature– Short metacarpals
Neuromuscular excitability
– NM depression– Arrythmias
Excitation-contraction– High BP– Cardiac arrest
Other– Bones, stones, abdo
groans, and psychic moans
– Polyuria / polydipsia
High Low
Ca - regulation
• Inverse relationship with P activates regulatory mechanisms
• To increase Ca1. PTH – bones, kidneys2. Calcitriol (activated vitamin D) – GI tract,
bones
• To decrease Ca1. Calcitonin
Low plasma Ca
Parathyroid glands
Increased PTH
Intestine
Kidneys
Increased activation of vitamin D
Increased Ca absorption
Increased plasma Ca
Increased Ca reabsorption
Increased Ca resorbed from bone
Increases responsiveness of bone to PTH
Bone
Note: low vitamin D also stimulates PTH release
Causes of hypercalcaemia
High intake / producti
on
10 HyperPTH Malignancy
Reduced excretio
n
Sarcoidosis / granulomatous diseases
Familial hypocalciuric hypercalcaemia
Other Paget’s disease Addison’s Drugs – lithium, antacids
Hypercalcaemia
Albumin normal/lowAlbumin raised
Urea raised
•Dehydration
Urea normal
•Cuffed specimen
ALP high
•Bone mets
•Sarcoid
•Hyperthyroid
P low/norm
Urea normal
•10/tertiary hyperPTH
P high/norm
ALP normal
•Myeloma
•Vit D excess
•Sarcoid
Causes of hypocalcaemia
Low intake / producti
on
HypoPTH / pseudo / pseudopseudo
Vitamin D deficiency Hypomagnaesia
Redistribution
Osteomalacia Pancreatitis Hypoalbuminaemia
Other Chronic kidney disease Thyroid surgery Respiratory alkalosis Drugs, frusemide,
bisphosphonates
Treatment
Hypercalcaemia – • Treat underlying disease• Rehydration – saline• Diuretics• Bisphosphonate - pamidronate
Hypocalcaemia – • Treat underlying disease• Calcium +/- phosphate binders• Others = vitamin D
Ca – summary points
Phosphate (PO43-)
PO43- source, storage,
functions • Source: diet: meat and milk!• Storage: Bone, intracellular (10%),
extracellular (1%)• Transport: Bound to plasma proteins• Functions:
– In bone, cell membranes, nucleic acids, 2,3-DPG, ATP
– (Involved in) excretion of H in the kidney– High energy intracellular enzymatic functions – Main intracellular buffer – buffers CO2– In coagulation / immune systems cascades
PO43- regulation
• Inverse relationship with Ca activates regulatory mechanisms
– PO increased via • Calcitriol action in GI tract
– PO decreased by • PTH release
Low plasma P
Increased plasma Ca
Calcitriol
Increased intestinal P absorption
Increased P reab. From
kidneys
No change in plasma Ca
Increased plasma P
Decreased PTH
Increased intestinal Ca absorption
Kidneys
Decreased C reab. From
kidneys
Decreased urinary P loss
Increased urinary Ca loss
PO43- signs and
symptoms
Symptoms of low Ca
Component bone, cells, 2,3-DPG etc.– High BP– Bone pain
High Low
Symptoms of high Ca
Component bone, cells, 2,3-DPG etc.– Encephalopathy– Hallucinations– Arrhythmias– Muscle weakness– Bone pain
Causes of hyperphosphataemia
High intake / producti
on
Enemas / laxatives TPN Vitamin D excess
Reduced excretio
n
CKD HypoPTH Hypomagnaesia Drugs - bisphosphonates
Redistribution
Cellular insult – trauma, burns, exercise, chemotherapy
Acidosis
Other Acromegaly Thyrotoxicosis
Causes of hypophosphataemia
Low intake / producti
on
Poor diet Malabsorption - Crohns
Increased excretio
n
10 HyperPTH Antacids
Redistribution
Alkalosis Refeeding syndrome Catecholamines Insulin
Other Steroids Alcoholism
Treatment
Hyperphosphataemia – • Dietary restriction• Phosphate binders – e.g. Ca carbonate• Enhance excretion via dehydration with
saline and diuresis with diuretic, e.g. furosomide
• If necessary, control, hyperparathyroidism – vitamin D metabolites
Hypophosphataemia –1.Treat underlying cause2.Oral or in some circumstances, IV P3.+/- vitamin
P – summary points
Magnesium (Mg2+)
Mg2+ source, storage, functions
• Source: diet• Storage: 2/3 bone, 1/3 intracellular, <1% plasma• Transport: ionised, plasma proteins, anion
complexes• Functions:
– Numerous – Muscle / nerve activity, vasomotor tone, cardiac excitability, catecholamine depressant
– Neuromuscular depression - CNS function– K regulation - PTH release– Coagulation
Mg2+ signs and symptoms
Cardiovascular excitability– Bradycardia (BP)– Heart block– Arrest
Neuromuscular depression– Hyporeflexia– Facial paraesthesia
CNS function– Coma– Respiratory
depression and apnoea
Coagulation– Increased coagulation
time
High Low
Cardiovascular excitability– Arhythmias– Cardiac arrest
Neuromuscular depression– Tetany– Paraesthesia
CNS function– Fits
Coagulation– Increased coagulation
time
Mg2+ regulation
• Mg2+ derangements uncommon• Relationship between Mg2+,
Ca2+ and K • Mg levels determined by:
1. Kidneys2. PTH – kidney, intestine, bone3. Insulin
Causes of hypermagnaesia
High intake / producti
on
Iatrogenic Drugs (esp. antacids) haemodialysis
Reduced excretio
n
Renal failure Drugs (lithium) Familial hypocalciuric
hypercalcaemia
Other Hypothyroidism Addisons Disease Depression
Causes of hypomagnaesia
Low intake / producti
on
Reduced dietary intake (TPN) Intestinal malabsorption Alcohol
Increased excretio
n
Diarrhoea Drugs (diuretics)
Redistribution
(Keto)acidosis Alkalosis Severe illness
Other Endocrine disorders (hyperthyroidism, Conn’s)
Pancreatitis Alcoholism
Treatment
Hypermagnaesia – • Treat underlying cause• Calcium gluconate• Insulin
Hypomagnaesia –1.Treat underlying cause2.Magnesium salts PO or IV
Mg – summary points
Chloride
Cl- source, storage, functions
• Source: diet• Storage: primarily extracellular
• Functions: – Maintenance of serum osmolality (together with cations, Na
and K) and ECF volume– Nerve conduction– Key constituent of HCl (thus helps activate intrinsic factor)– Regulation of carbon dioxide transport in erythrocytes and
thus Ph– Control of acid-base balance - Cl acts as buffer
• No specific symptoms associated with Cl derangements (alkalosis = exception)
• Cl regulation is achieved by the kidneys
Causes of hyperchloraemia
High intake / producti
on
Excessive ingestion of high salt diets (CCF patients)
Reduced excretio
n
Kidney failure
Causes of hypochloraemia
Low intake / producti
on
(Infants) chloride deficient formulas
Other • Water overload• Wasting conditions• Extensive body burns • Systemic acidosis
Case study 1
• XX man post operation. Received X ml/Ls 5% dextrose post operatively
• You are the SHO bleeped because he’s collapsed in trying to get out of the bed to go to the toilet. He’s nauseous, has a headache and seems a little groggy– What may be the problem?– What may have caused it?– How may it be avoided?
Case study 2
• XX year old woman found on the floor by her husband. She is confused, weak and reports that she’s nauseous. In trawling through her notes, you see she’s well known to the hospital given her extensive psychiatric Hx, noting that four months ago, she was diagnosed with lung cancer.
• Her chemistry results show that she’s hyponatraemic.
• What could be the cause?• What test would you like to do next?
Case study 2 continued
• Her test results show:• Urine >500mosmol/kg (high)• So what has she got?
Case study 3
• You are asked to see a patient whom has been admitted on the ward via GP referral after a series of very high Cr results (>800mmol/L). He is known to the hospital and has a long history gout.
• What may his condition be?• What sort of imbalances would you expect in a
patient with this condition? (High or Low)– Na - K– Ca - Phosphate– PTH - Hb– Ph
Day 2
Renal function tests (Na, K, creatinine + urea
for completeness)
Urea source, storage, functions
• Source: amino acids (AA)– AAs catabolised to ammonium and then into urea
in the liver via the ornithine cycle – Urea = major mechanism to eliminate ammonia
(extremely toxic)– Urea is transported to the kidneys for excretion
• Function:– Mechanism to eliminate ammonia – Contributes to the renal countercurrent
mechanism– Used as a marker of GFR
Urea signs and symptoms
• General: nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, thirst, uraemic fetor
• Neurological: encephalopathy, visual disturbances
• Dermatological: pruritus, uraemic frost, sallowness
• Cardiovascular: uraemic pericarditis• +other renal failure signs/symptoms• Uraemia can progress to death
High (uraemia)
Urea regulation
• Urea level = amount of protein catabolism – excretion by kidneys
• Uraemia = clinical syndrome resulting from severe kidney dysfunction
Causes of high urea
High intake / producti
on
• High protein diet• GI bleeding, catabolism, sepsis,
surgery = a high protein ‘meal’• Drugs- steroids
Reduced excretio
n
• Dehydration• Kidney failure (all causes) • Drugs – tetracyclines,
nephrotoxics
Causes of low urea
Low intake / producti
on
• Liver disease• Malnutrition / decreased
protein intake / prolonged IV • Pregnancy
Treatment
High urea – • Treat underlying cause• Example in metabolic disorders:
– 1.Dietary protein limitation– 2.Increased ammonia secretion
(levulose / antibiotics)– 3. Replacing missing urea cycle
constituents
Cr source, functions
• Source: by-product of muscle metabolism
• Function: marker of kidney function (GFR)
• Regulation: – Kidney – freely filtered at glomerulus, only
slightly re-absorbed. Limited secretion.– Steadily excreted compared to urea
• Decreased GFR = increased secretion• ‘No muscle’ patients = ‘false’ low Cr reading despite low
GFR
• No known symptoms associated with high Cr
Causes of high CrHigh intake / producti
on
• Diet• Race (Afro Caribbean• Body-builders• Drugs – steroids• Muscle injury
Reduced excretio
n
• Renal failure• Drugs:
– trimethoprim, sulphamethoxazole etc.
Other • Drugs – interfere with assay for Cr
• Rheumatoid arthritis
Causes of low Cr
Low intake / producti
on
• increasing age - age-related decline in muscle mass
• females - reduced muscle mass
• malnutrition/ muscle wasting/ amputation - reduced muscle mass ± reduced protein intake
• vegetarian diet - decrease in creatinine generation
RFTs – summary points
Liver function tests (ALT, ALP, bilirubin and
albumin)
+ AST, gGT, total protein for completeness
LFT overview
• LFTs = more than the liverRole:• Screen, confirm diagnosis, construct differential
diagnoses• Indicate prognoses• Monitor progress and response to therapyProblems:• Single liver tests not clinically useful
– Serious liver diseases can have normal levels – ‘Benign’ situations can cause transitory
derangements– Many diseases similar LFT profile
LFT parameters
• LFTs assess various aspects of the biliary tract structure and functionUptake, conjugation & excretion of anionic compounds
Serum total bilirubinBile acidsUrinary bilirubin (also urobilinogin)
Synthetic functionSerum albumin Serum proteinsINR / APTT
Hepatocellular damageASTALTSerum ferritinB12ALPGGT
ALT/AST source, transport & functionSource:
• ALT – cytosolic enzyme– most specific to liver (also in kidneys, muscle,
heart)• AST
– mitochondrial enzyme (think high energy)– in liver, heart, kidneys, muscle, brain, red cells
and pancreasTransport:• Released into blood when hepatocytes damagedFunction:• ALT: role in processing of proteins• AST: role in metabolism
ALT/AST derangements
• ALT: levels may be misleading– Normal/low levels in compensated
cirrhosis– Raised by heavy drinking
• Generally:– hepatocellular injury = very high– Obstructive jaundice = mildly high
• ALT/AST ratio unreliable guide to diagnosis
Causes of ALT/AST derangements
• Liver - acute hepatitis, cirrhosis, neoplasia, haemochromatosis, alcoholic liver disease
• Biliary duct pathologies – cholestasis• Heart damage - MI, acute HF, myocarditis• Myopathies – Duchenne muscular
dystrophy, polymyositis• Kidney damage• Shock • Drugs – carbamazapine, paracetamol,
heparin etc.
LFTs principles of management
• Additional lab tests if Hx and exam don’t explain derangements
– (ALP / bilirubin should be part of the initial lab evaluation)
– ferritin, hepatitis A, B, and C serology etc.
– Prothrombin time (PT) / albumin – FBC
• Then treat underlying pathology
ALP source and derangements
Source: • Cannicular and sinusoidal membranes of the liver• Tissue specific isoenzymes also found in bone,
intestine, placenta High:• Liver / biliary tract diseases - obstruction,
malignancies• Bone - Paget’s, bone metastases, endocrine
abnormalities• Intestine – Crohns, UC• Placenta - pregnancy• Other – Normal, drugs, Hodgkins, polymylagia
rheumatica
ALP principles of management
• Of limited value to differentiate liver diseases; helpful to assess bone-related
• ALT hepatic or bony origin? (e.g. met breast Ca)
– Other tests: GGT, bone scan, Liver USS
gGT source, transport & function
Source:• Microsomal enzyme in many tissues: liver,
kidneys, pancreas, intestine and prostate. In liver, found in hepatocytes and biliary epithelial cells
Causes of derangements:• GGT = unreliable marker• Interpret gGT alongside other LFTs:
– Mild liver disease = ALT:AST >1 – anticipate raised gGT– Extensive liver disease tends = ALT:AST <1 – gGT
compatible with alcohol damage
• If AST/ALT normal, gGT indicates alcohol intake
gGT derangements
• Liver disease – cholestasis, hepatitis• Alcohol • Drugs – phenytoin, phenobarbitol and
other enzyme inducing drugs• Pancreatitis• Miscellaneous - MI, diabetes mellitus,
anorexia, Guillain Barre Syndrome, hyprthyroidism, neurological disease
Total plasma proteins source, transport &
functionTest: • Total protein = albumin + globulinSource:• Mostly liver. Also production outside liver
Function: • Proteins = building blocks of cells and tissues• (Alb) Maintenance of blood colloid oncotic
pressure: therefore volume and distribution of ECF • (Alb) Transportation of thyroid, adrenocortical and
gonadal hormones• (Globs) Antibodies, enzymes + other misc. proteins• Anions – provide 15% of buffering capacity of blood
Total protein derangements
High intake / producti
on
• Raised immunoglobulins– Autoimmune conditions –
RA, SLE– Genetic conditions – Cancer – myeloma
• Drugs – anabolic steroids, androgens, GH, insulin, progesterone
Other Dehydration Tourniquet left on
Total protein derangements
Low intake / producti
on
Liver disease (cirrhosis) Malabsorption syndromes –
coeliac, post bowel resection
Increased excretio
n
Kidney disorders – diabetes, hypertension, glomerulonephridites
GI Tract loss Burns / exudative skin disease Inflammatory states Diuretics
Other Dilutional - Fluid retention, SIADH, IV fluids
Increased catabolism – injury, post op.
Bilirubin – source, transport
• Source – pigment resulting from blood breakdown
• Transport– Unconjugated, insoluble bilirubin bound
to albumin– Conjugated bilirubin ‘free’ – if raised,
more joins to albumin
Mature red cells
Bilirubin
Bile released
Conjugated bilirubin
glucoronysl transferase
Bilirubin + glucoronic acid
Iron/globin removed from haem
Biliverdin
Stercobilin or urobilinogen
Reticuloendothelial system
Albumin
Hyperbilirubinaemia - causes
UNconjugated ConjugatedExcessive production Hepatocellular
abnormalities (unconjugated sometimes)
Ineffective haemopoesis Haemolytic disorders
• Primary hepatocyte disease: cirrhosis, hepatitis, malignancies, drug reactions, iron overload Pregnancy Postoperative jaundice
Abnormal bilirubin metabolism (congenital)
Obstructive
Enzyme system immaturity: newborn jaundice Inherited defects: Gilbert’s Crigler-Najjar syndrome, drugs
• Calculi• Neoplasms• Strictures• Atresia
Hyperbilirubinaemia – symptoms
• Jaundice• Tiredness• Abdominal pain• Weight loss• Vomiting• Fever• Itchy• Dark urine• Pale stools
Amylase - source• Source: pancreas (as distinct from salivary amylase)• Functions:
– Carbohydrate digestion– Differentiates acute pancreatitis from other causes
of the acute abdomen (unreliable)>400 U/L• Acute pancreatitis: rises quickly, returns to
normal in ~ 4 days<400 U/L• Acute peritonitis: elevates amylase. Usually not
above 400 U/L. • Chronic pancreatitis does not raise amylase.
Acute on chronic exacerbation may
HyperamylasaemiaGI Acute pancreatitis – also pancreatic pseudocysts,
abscesses,pancreatic trauma Peritonitis AAA Acute mesenteric infarctions Perforated duodenal ulcers Intestinal obstructions Acute appendicitis Liver metastases, also biliary tract diseases
Other Malignancies - Ovarian / Prostatic, Lung Renal failure CCF Alcohol DKA Drugs – optiates, azathioprine etc. Septicaemia
LFTs – summary points
Great resources
• World Anaesthesia online – great stuff on physiology, http://www.nda.ox.ac.uk/wfsa/index.htm
• Ye olde OHCM ‘clinical chemistry’ section